lecture 12 kemp
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| berry aneurysm | saccular outpouching of vessel wall located in the circle of Willis; usually an expansion of a congenitally weak wall
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| arteriosclerosis | hardening of the arteries, thickening and loss of elasticity of the vessel wall
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| 3 forms of arteriosclerosis | atherosclerosis, arteriolosclerosis, Mönckeberg medial calcification
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| major non-modifiable risk factors of atherosclerosis | age (older is worse), sex (men have higher risk, post-menopausal women are similar), genetics (familial hypercholesterolemia increases risk of MI, stroke, etc.)
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| major modifiable risk factors of atherosclerosis | hyperlipidemia (high LDL), HTN, DM (induces hyperchol'emia), cigarette smoking (1 ppd for yrs inc risk 200%)
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| additional risk factors for atherosclerosis | elevated CRP is marker for complications of atherosclerosis, lipoprotein A competes with plasmin activity, lack of excercise, stress, obesity, hyperhomocystinemia
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| intimal thickening | endothelial injury is caused by toxins in smoke, chol, infectious agents of hemodynamic disturbances. smooth muscle cells move from media to intima and start proliferating, causing intimal thickening
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| fatty streak | linear and slight elevations in the intima that are filled with lipid-laden foam cells (macrophages that ingested oxidized LDL); precursor to plaque
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| pathogenesis of atherosclerotic plaques | disturbances in endothelium caused by turbulent flow, LDL + ROS = squelch NO, toxic to endothelial and smooth muscle cells. monocytes/macrophages eat lipid and make more ROS further insulting endothelium and adding to plaque formation
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| atherosclerotic plaque | eccentric mass lesion that can obstruct the lumen of an artery; contains SM cells, macrophages and T cells, EC matrix and lipid. are neovascularized, variable calcifications. components are: fibrous cap, shoulder and necrotic core
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| complications of atherosclerosis | acutely: rupture, ulceration or erosion of the plaque will promote thrombosis and expansion of plaque size or occlusion of lumen // chronic: pressure of plaque atrophies media, can result in aneurysm that's prone to rupture
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| how plaque size changes over time (chronic change) | increasing accumulation of LDL, continued production of collagen and/or resolution of hemorrhage
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| claudication | like angina, but in the BLE - due to ischemia of musculature during exercise, ceases with rest
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| areas where atherosclerosis can result in pathology | MI, stroke, PVD, mesenteric ischemia or infarction of organs, claudication
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| 2 most important contributors to (dys)regulation of BP | blood volume (CO, due to sodium conc'n, much up to RAAS) and peripheral resistance (controlled by arterioles, balance btwn vasoconstrictors and -dilators, also angiotensin II effect)
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| RAAS | renin from JGA cells in kidney when pressure is low/vol reduced; renin makes angiotensin I to AII in lungs, which inc PVR and BP; aldosterone release causes retention of Na/H2O raising BP and blood vol
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| renal causes of HTN | AGN, chronic renal dz, renal artery stenosis (one kidney thinks BP is low, releases renin causing global HTN), renin-producing tumors
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| endocrine causes of HTN | hyper- or hypothyroidism, pheochromocytoma, exogenous hormones, Cushing syndrome, primary hyperaldosteronism (tumor of adrenal cortex)
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| CV causes of HTN | coarctation of aorta, aortic stenosis and increased CO, increased blood vol
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| neurologic causes of HTN | stress, psychogenesis, increased ICP (brain feels pressure is low b/c vessels are constricted)
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| hyaline arteriolosclerosis | tiny microinfarcts replaced by hyaline deposits that are thick, acellular and eosinophilic. SM cells overproduce ECM; benign HTN
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| hyperplastic arteriolosclerosis | SM cells thicken and BM is duplicated, concentric and laminated thickening like onion skin; malignant HTN
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| important causes of aneurysms | atherosclerosis and cystic medial degeneration, syphilis infection or other bacteria - mycotic aneurysms, trauma
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| syphilitic aneurysm | involve the thoracic aorta including aortic root commonly; pathogen obliterates vaso vasorum and causes medial ischemia, weakening the wall and allowing for aneurysm formation
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| AAA pathogenesis | initimal plaques can compress the vasculature of the media and lead to infarct & necrosis. proteolysis by metalloproteinases, aortic wall inflammation, oxidative stress are big 3 factors
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| clinical complications of AAA | rupture & hemorrhage, obstructing a branch like the mesenteric aa., emoblizaion of thrombus or plaque fragment, compression of adj structures, abd mass formation
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| aortic dissections | usually due to HTN, rupture in intima allows blood to flow into vessel layers. mortality rate is high, rupture or hemorrhage can cause huge bleeds, aortic insufficiency, MI or sudden death
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| common pathogenic mechanisms of vasculitis | infections and immune-mediated inflammation by immune complex formation, anti-neutrophil or anti-endothelial Abs
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| arteriolar nephrosclerosis | caused by systemic HTN that affects the kidney's arterioles and causes fibrinous exudates on surface that appear granular grossly
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| primary HTN | systemic HTN with no known underlying cause, aka idiopathic or essential HTN
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| secondary HTN | HTN due to some known cause like neuroendocrine tumor, renal artery stenosis or coarctation of aorta
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| aneurysm | abnormal dilation of the wall of a
blood vessel or heart
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| true vs false aneurysm | true - dilation of all 3 layers of the vessel wall vs false - hematoma outside the wall of the vessel, it's confined to an area so it appears to be dilation of the vessel wall
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| saccular | eccentric outpouching of vessel wall involving only a segment of the wall
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| fusiform | generalized, concentric dilation of the wall of the vessel
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| mycotic aneurysm | due to infection of bacteria like Salmonella, cause suppurative inflammation of the media, bacteria in bloodstream directly infect arterial walls
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| aortic dissection | tearing of the intima allows blood to enter the media of the vessel and travel within it
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| cystic medial degeneration | seen in Marfan syndrome, areas of aortic aneurysm: elastic tissue is fragmented and separated by an amorphous and acellular proteoglycan-rich ECM
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| Raynaud phenomenon | exaggerated vasoconstriction of arterioles and arteries in the digits. can be primary and due to cold or emotion in young women or secondary due to other dz like SLE or atherosclerosis
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| varicose veins | dilated veins produced by increased intraluminal pressure or loss of vessel wall support
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| thrombophlebitis | inflammation and thrombosis of veins
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| triad of Wegener granulomatosis | acute necrotizing granulomas of upper resp tract, vasculitis in lungs and focal or crescentic glomerulonephritis
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| esophageal varices | due to livver cirrhosis and congestion of portal vein; esophageal veins are alternate route of return of blood to heart bypassing fibrotic liver. dilation can cause rupture and fatal hemorrhage
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| hemorrhoids | caused by prolonged vascular congestion from straining with BMs or preg; fates: thrombose, hemorrhage, will be painful
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| causes of thoracic aortic aneurysm | Syphilis, bicuspid aortic valve, Marfan syndrome,
vasculitis (Giant cell arteritis, Takayasu arteritis
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| Buerger dz aka thromboangiitis obliterans | medium, small vessels (esp. tibial/radial), segmental and acute vasculitis with luminal thrombses and microabscesses. < 35 y/o, heavy smokers, painful phlebitis, idiosyncratic immune response
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| polyarteritis nodosa vs microscopic polyangiitis | exactly the same except MP involves lung, has temporally similar lesions and shows p-ANCA positivity vs PAN being Hep B immune complexes
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| 3 types of hemangiomas | cavernous (large spaces filled with blood and lined by bland endothelial cells), capillary (superficial & tightly packed with small vascular channels) and pyogenic granulomas
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| telangiectasia | dilated pre-existing capillaries and veins in places like oral MM, organs and skin
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| bacillary angiomatosis | vascular proliferations in the skin, bone and brain due to infection with Bartonella spp.
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| types of Kaposi sarcoma | chronic (Eastern European older men on BLE, not a/w HIV), lymphadenopathic (Africa, aggressive neoplasm), transplant-associated (solid organs, aggressive neoplasm), AIDS-associated (very aggressive)
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| Kaposi sarcoma etiology | caused by infection with human Herpesvirus 8
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| Kaposi sarcoma morphology | patches then plaques then nodules at final stage. microscopically: angulated blood vessel with extravasated RBCs
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| angiosarcoma | tumors from well-differentiated to poor, hepatic angiosarcomas & vinyl chloride use, in setting of lymphedema as in breast ca pts post-axillary lymphadenectomy
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